Search results for "NFOL"

showing 10 items of 144 documents

Endoplasmic Reticulum Stress Inhibition Protects against Excitotoxic Neuronal Injury in the Rat Brain

2007

Elevated brain glutamate with activation of neuronal glutamate receptors accompanies neurological disorders, such as epilepsy and brain trauma. However, the mechanisms by which excitotoxicity triggers neuronal injury are not fully understood. We have studied the glutamate receptor agonist kainic acid (KA) inducing seizures and excitotoxic cell death. KA caused the disintegration of the endoplasmic reticulum (ER) membrane in hippocampal neurons and ER stress with the activation of the ER proteins Bip, Chop, and caspase-12. Salubrinal, inhibiting eIF2α (eukaryotic translation initiation factor 2 subunit α) dephosphorylation, significantly reduced KA-induced ER stress and neuronal deathin vivo…

PERKMaleKainic acidProgrammed cell deathcaspase-12ExcitotoxicityBiologymedicine.disease_causeEndoplasmic ReticulumHippocampusCalcium in biologyeIF2 alphaSalubrinalchemistry.chemical_compoundsalubrinalmedicineExcitatory Amino Acid AgonistsAnimalsRats WistarNeuronsKainic AcidhippocampuGeneral NeuroscienceEndoplasmic reticulumGlutamate receptorBrainNeural InhibitionArticlesCell biologyRatsOxidative StresschemistryUnfolded protein responseNeuroscience
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The energy spectrum of atmospheric neutrinos between 2 and 200 TeV with the AMANDA-II detector

2010

The muon and anti-muon neutrino energy spectrum is determined from 2000-2003 AMANDA telescope data using regularised unfolding. This is the first measurement of atmospheric neutrinos in the energy range 2 - 200 TeV. The result is compared to different atmospheric neutrino models and it is compatible with the atmospheric neutrinos from pion and kaon decays. No significant contribution from charm hadron decays or extraterrestrial neutrinos is detected. The capabilities to improve the measurement of the neutrino spectrum with the successor experiment IceCube are discussed.

Particle physicsAMANDA[PHYS.ASTR.HE]Physics [physics]/Astrophysics [astro-ph]/High Energy Astrophysical Phenomena [astro-ph.HE]Physics::Instrumentation and Detectors[SDU.ASTR.CO]Sciences of the Universe [physics]/Astrophysics [astro-ph]/Cosmology and Extra-Galactic Astrophysics [astro-ph.CO]Solar neutrinoAstrophysics::High Energy Astrophysical PhenomenaAMANDA; Atmospheric neutrinos; Cherenkov radiation; Neural net; Unfoldingneural netFOS: Physical sciencesAetiology screening and detection [ONCOL 5]01 natural sciences7. Clean energy[PHYS.ASTR.CO]Physics [physics]/Astrophysics [astro-ph]/Cosmology and Extra-Galactic Astrophysics [astro-ph.CO]0103 physical sciences010306 general physicsunfoldingPhysicsHigh Energy Astrophysical Phenomena (astro-ph.HE)Muon010308 nuclear & particles physics[SDU.ASTR.HE]Sciences of the Universe [physics]/Astrophysics [astro-ph]/High Energy Astrophysical Phenomena [astro-ph.HE]Cherenkov radiationHigh Energy Physics::PhenomenologyAstronomy and AstrophysicsSolar neutrino problematmospheric neutrinosCosmic neutrino backgroundNeutrino detectorddc:540Measurements of neutrino speedHigh Energy Physics::ExperimentAstrophysics::Earth and Planetary AstrophysicsNeutrino astronomyNeutrinoAstrophysics - High Energy Astrophysical Phenomena
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Nutritional assessment in preterm infants with special reference to body composition

2001

In recent years, improvements in care have significantly improved survival in preterm and, particularily, the very low birth weight infant (VLBW). While immediate survival can be directly related to pulmonary maturity, several studies stress the importance of timely and adequate nutrition in these high-risk infants on a short- and long-term [1]. Yet, nutritional support remains a very controversial issue in these high-risk infants. Early provision of adequate intakes may be limited by clinical instability and immaturity. At the same time, nutritional requirements and methods of nutritional assessment are not well defined. The aim of this paper is to outline some of the methods used during n…

Pediatricsmedicine.medical_specialtybusiness.industryBody WeightInfant NewbornImproved survivalBody HeightSkinfold ThicknessLow birth weightAbsorptiometry PhotonNutrition AssessmentAnimals NewbornBone DensityPediatrics Perinatology and Child HealthBody CompositionmedicineAnimalsHumansmedicine.symptomEnergy MetabolismInfant Nutritional Physiological PhenomenabusinessWeight gainInfant PrematureSeminars in Neonatology
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Mitochondrial (dys)function - a factor underlying the variability of efavirenz-induced hepatotoxicity?

2015

Background and Purpose The non-nucleoside analogue reverse transcriptase inhibitor efavirenz is associated with hepatic toxicity and metabolic disturbances. Although the mechanisms involved are not clear, recent evidence has pinpointed a specific mitochondrial action of efavirenz accompanied by the induction of an endoplasmic reticulum (ER) stress/unfolded protein response in human hepatic cells. The aim of this study was to further investigate the involvement of this organelle by evaluating efavirenz's effects in cells lacking functional mitochondria (rho°) and comparing them with those of the typical mitotoxic agent rotenone, a standard complex I inhibitor, and the ER stress inducer thaps…

PharmacologyThapsigarginEfavirenzReverse-transcriptase inhibitorEndoplasmic reticulumRotenoneBiologyMitochondrionPharmacologychemistry.chemical_compoundchemistryUnfolded protein responseHepatic stellate cellmedicinemedicine.drugBritish Journal of Pharmacology
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Antitumor effects of dehydroxymethylepoxyquinomicin, a novel nuclear factor-kappaB inhibitor, in human liver cancer cells are mediated through a reac…

2009

Activation of the nuclear transcription factor-kappa B (NF-kappa B) has been implicated in liver tumorigenesis. We evaluated the effects of a novel NF-kappa B inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), in two human liver cancer cell lines HA22T/VGH and HuH-6. DHMEQ treatment dose dependently decreased the DNA-binding capacity of the NF-kappa B p65 subunit, inhibited cell growth and proliferation, and increased apoptosis as shown by caspase activation, release of cytochrome c, poly(ADP-ribose) polymerase cleavage, and down-regulation of survivin. DHMEQ also induced a dose-dependent activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling, …

Programmed cell deathCarcinoma HepatocellularBIOLOGICAL-ACTIVITIESDrug Evaluation PreclinicalDown-RegulationAntineoplastic AgentsApoptosisBiologymedicine.disease_causeACTIVATIONchemistry.chemical_compoundHYDROGEN-PEROXIDEENDOPLASMIC-RETICULUM STRESSCell Line TumorSurvivinNADPH OXIDASEmedicineHumansOXIDATIVE STRESSProtein kinase AEndoplasmic Reticulum Chaperone BiPINDUCED APOPTOSISCell ProliferationPharmacologySettore MED/12 - GastroenterologiaDose-Response Relationship DrugUNFOLDED PROTEIN RESPONSECell growthCyclohexanonesINDUCTIONLiver NeoplasmsDEATHNF-kappa BCytochromes cMolecular biologyCell biologyEnzyme ActivationchemistryApoptosisCaspasesCancer cellBenzamidesSettore BIO/14 - FarmacologiaMolecular MedicineGrowth inhibitionMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesOxidative stressMolecular pharmacology
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ROS-Dependent ER Stress and Autophagy Mediate the Anti-Tumor Effects of Tributyltin (IV) Ferulate in Colon Cancer Cells

2020

Organotin compounds represent potential cancer therapeutics due to their pro-apoptotic action. We recently synthesized the novel organotin ferulic acid derivative tributyltin (IV) ferulate (TBT-F) and demonstrated that it displays anti-tumor properties in colon cancer cells related with autophagic cell death. The purpose of the present study was to elucidate the mechanism of TBT-F action in colon cancer cells. We specifically show that TBT-F-dependent autophagy is determined by a rapid generation of reactive oxygen species (ROS) and correlated with endoplasmic reticulum (ER) stress. TBT-F evoked nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant response and Nrf2 silenc…

Programmed cell deathNF-E2-Related Factor 2Glucose-regulated proteinApoptosismedicine.disease_causeArticleCatalysisInorganic Chemistrylcsh:ChemistrySettore BIO/10 - BiochimicaAutophagyTumor Cells CulturedmedicineHumansGene silencingoxidative stressPhysical and Theoretical ChemistryEndoplasmic Reticulum Chaperone BiPMolecular Biologylcsh:QH301-705.5tributyltin (IV) derivativeSpectroscopyCell Proliferationoxidative strebiologyChemistryEndoplasmic reticulumOrganic ChemistryAutophagyCancerROSGeneral Medicineendoplasmic reticulum stremedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999autophagic cell deathColonic NeoplasmsUnfolded protein responseCancer researchbiology.proteinendoplasmic reticulum stressTrialkyltin CompoundsReactive Oxygen SpeciesOxidative stress
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Bax inhibitor-1 is likely a pH-sensitive calcium leak channel, not a H+/Ca2+ exchanger.

2014

The endoplasmic reticulum (ER) plays a key role in the synthesis, folding, and sorting of proteins, and disturbances of this delicate system can cause cell death. The ER also serves as the major intracellular calcium (Ca(2+)) store, and release of Ca(2+) from this store controls diverse cellular functions. At the interface of both these functions of the ER is Bax inhibitor-1 (BI-1), an evolutionarily conserved multifunctional protein that mediates Ca(2+) efflux from the ER and protects against ER stress. Several mechanisms have been proposed to explain how BI-1 might mediate Ca(2+) efflux from the ER. Chang et al. present structural evidence that a bacterial homolog of BI-1, BsYetJ, is a pH…

Programmed cell deathProtein familyProteolipidschemistry.chemical_elementCalciumBiologyEndoplasmic ReticulumBiochemistryModels BiologicalCalcium in biologySpecies SpecificityHumansMolecular BiologyBAX inhibitor 1Endoplasmic reticulumCell MembraneMembrane ProteinsCell BiologyHydrogen-Ion ConcentrationCell biologychemistryUnfolded protein responseCalciumEffluxCalcium ChannelsApoptosis Regulatory ProteinsBacillus subtilisScience signaling
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Coupling Endoplasmic Reticulum Stress to the Cell Death Program

2002

Accumulation of misfolded proteins and alterations in Ca2+ homeostasis in the endoplasmic reticulum (ER) causes ER stress and leads to cell death. However, the signal-transducing events that connect ER stress to cell death pathways are incompletely understood. To discern the pathway by which ER stress-induced cell death proceeds, we performed studies on Apaf-1−/− (null) fibroblasts that are known to be relatively resistant to apoptotic insults that induce the intrinsic apoptotic pathway. While these cells were resistant to cell death initiated by proapoptotic stimuli such as tamoxifen, they were susceptible to apoptosis induced by thapsigargin and brefeldin-A, both of which induce ER stress…

Programmed cell deathThapsigarginbiologyEndoplasmic reticulumCytochrome cIntrinsic apoptosisCell BiologyBiochemistryCell biologychemistry.chemical_compoundchemistryApoptosisbiology.proteinUnfolded protein responseMolecular BiologyCaspaseJournal of Biological Chemistry
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Highlighting curcumin-induced crosstalk between autophagy and apoptosis: A biochemical approach coupling impedancemetry, imaging, and flow cytometry

2019

Curcumin, a major active component of turmeric (Curcuma longa, L.), is known to have various effects on both healthy and cancerous tissues. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying the anticancer effects of curcumin is still unclear. Since there is a consensus about endoplasmic reticulum (ER) stress being involved in the cytotoxicity of many natural compounds, we investigated by Amnis ® Imaging flow cytome-try the mechanistic aspects of curcumin's destabilization of the ER, but also the status of the lysosomal compartment involved in curcumin-associated apoptosis. Curcumin induces ER stress thereby causing an un…

Programmed cell death[SDV]Life Sciences [q-bio][SDV.TOX.TVM]Life Sciences [q-bio]/Toxicology/Vegetal toxicology and mycotoxicology[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Mitochondrion03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biology0303 health sciencesChemistryAutophagy[SDV.BBM.MN]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular Networks [q-bio.MN]Cell cycle3. Good healthCell biology[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsApoptosis030220 oncology & carcinogenesis[SDV.TOX]Life Sciences [q-bio]/ToxicologyCancer cellUnfolded protein responseCurcumin
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Highlighting Curcumin-Induced Crosstalk between Autophagy and Apoptosis as Supported by Its Specific Subcellular Localization

2020

Curcumin, a major active component of turmeric (Curcuma longa, L.), is known to have various effects on both healthy and cancerous tissues. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying the anticancer effect of curcumin is still unclear. Since there is a recent consensus about endoplasmic reticulum (ER) stress being involved in the cytotoxicity of natural compounds, we have investigated using Image flow cytometry the mechanistic aspects of curcumin&rsquo

Programmed cell deathautophagyCell Membrane PermeabilityCurcumin[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Article03 medical and health scienceschemistry.chemical_compound0302 clinical medicineLysosomeCell Line TumorxCELLigencemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Humanscancerlcsh:QH301-705.5030304 developmental biologyreal-time cellular impedanceCell Nucleus0303 health sciencescalciumEndoplasmic reticulumAutophagyapoptosisROSGeneral Medicine3. Good healthCell biologyMitochondriaendoplasmic reticulummedicine.anatomical_structurecell deathchemistrylcsh:Biology (General)Apoptosis030220 oncology & carcinogenesisCancer cellCurcuminUnfolded protein responseUnfolded Protein ResponselysosomeLysosomes[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologySubcellular Fractions
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